Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinically, we most often associate Wernicke's encephalopathy (WE) with an alcohol abusing population. However, it is important to consider other causes of malnutrition and vitamin deficiency as risk factors for the development of this disorder. We present a case of a 51-year-old man with schizophrenia and malnutrition who presented with delirium, ophthalmoplegia, and seizures. He responded rapidly to the administration of IV thiamine. Because of the high rate of mortality and morbidity, WE should be high on the differential of any patient at risk for malnutrition or with ophthalmoplegia, regardless of alcohol history. This is particularly important in psychiatric patients where the syndrome may be masked and thus treatment delayed.
J Gen Intern Med 2006 Dec
PMID:Wernicke's encephalopathy in a patient with schizophrenia. 1692 99

The effects of ethanol on epilepsy are very complex. Ethanol can have depressant as well as excitatory effect on different animal models of epilepsy. Systemic administration of homocysteine can trigger seizures. The aim of the present study was to examine the changes of total spectral power density after ethanol alone and together with homocysteine thiolactone in adult rats. Adult male Wistar rats were divided into following groups: 1. saline-injected, (control) C; 2. D, L-homocysteine thiolactone, H (8 mmol/kg); 3. ethanol, E (E(0.5), 0.5 g/kg; E(1), 1 g/kg; E(2), 2 g/kg) and 4. E (E(0.5), E(1), and E(2)) 30 min prior to H, EH (E(0.5)H, E(1)H and E(2)H). For EEG recordings three gold-plated screws were implanted into the skull. Our results demonstrate that ethanol, when applied alone, increased total EEG spectral power density of adult rats with a marked spectrum shift toward low frequency waves. In EH groups, increasing doses of ethanol exhibited a dose-dependent effect upon spectral power density. Ethanol increased EEG spectral power density in E(0.5)H and E(1)H group, comparing to the H group (p > 0.05), the maximal increase was recorded with the lowest ethanol dose applied. The highest dose of ethanol (E(2)H) significantly decreased total power spectra density, comparing to the H group. We can conclude that high doses of ethanol depressed marked increase in EEG power spectrum induced by D,L-homocysteine thiolactone.
Gen Physiol Biophys 2009
PMID:High dose of ethanol decreases total spectral power density in seizures induced by D,L-homocysteine thiolactone in adult rats. 1989 76

We investigated the rat brain activity in acute seizures evoked by camphor essential oil or its main constituent 1,8-cineole by wavelet (primarily) and fractal analysis. Experiments were performed on anesthetized animals before and after intraperitoneal camphor oil or cineole administration. The properties of frequency bands in pre-ictal, ictal and inter-ictal stages have been determined by wavelet analysis. The domination of delta frequency band was confirmed in obtained brain activities, which participate with approximately 45% of mean relative wavelet energy (MRWE) in control signals and arise up to approximately 76% MRWE in energy spectrum during the ictal stage (after drug administration). Other frequency bands decreased during ictal stage and arised in inter-ictal stage. There was a dosedependent response of cineole effect: increase in cineole concentration leaded to the higher values of relative wavelet energy (RWE) of delta frequency band while there were slight changes of the mean fractal dimension (FD) values as a measure of system complexity.
Gen Physiol Biophys 2009
PMID:Wavelet and fractal analysis of rat brain activity in seizures evoked by camphor essential oil and 1,8-cineole. 1989 77

The aim of our study was to test the hypothesis, if melatonin pre-treatment (in dose of 100 mg/kg) can influence the changes of brain function after short-term hypoxia exposition (simulated altitude 9000 m) in young immature rats. Experiments were performed on freely moving 12-, 25- and 35-day-old male Wistar rats. One hour prior to hypoxia exposition, animals were pre-treated with melatonin and 24 hours after hypoxia cortical afterdischarges (ADs) were elicited by repeated stimulation of the right sensorimotor cortex. The duration of evoked ADs and shape of evoked graphoelements was monitored. Short-term exposure to hypoxic conditions resulted in significantly shorter ADs duration in 12-day-old rats after stimulations (except the 2nd one stimulation) compared to control group. Administration of melatonin prolonged the duration of ADs after all stimulations except the 1st one. Analysis of the duration ADs revealed no significant changes, either after the exposition to hypobaric hypoxia or after melatonin administration in 25- and 35-day-old animals. Effects and mechanisms of melatonin action on the brain seizure susceptibility and the possible beneficial role of that treatment in hypoxic brain damage are discussed.
Gen Physiol Biophys 2010 Mar
PMID:Melatonin modulates hypoxia-induced changes of rat brain excitability. 2037 82

Free polyunsaturated fatty acids (PUFAs) modulate the voltage dependence of voltage-gated ion channels. As an important consequence thereof, PUFAs can suppress epileptic seizures and cardiac arrhythmia. However, molecular details for the interaction between PUFA and ion channels are not well understood. In this study, we have localized the site of action for PUFAs on the voltage-gated Shaker K channel by introducing positive charges on the channel surface, which potentiated the PUFA effect. Furthermore, we found that PUFA mainly affects the final voltage sensor movement, which is closely linked to channel opening, and that specific charges at the extracellular end of the voltage sensor are critical for the PUFA effect. Because different voltage-gated K channels have different charge profiles, this implies channel-specific PUFA effects. The identified site and the pharmacological mechanism will potentially be very useful in future drug design of small-molecule compounds specifically targeting neuronal and cardiac excitability.
J Gen Physiol 2011 Jun
PMID:An electrostatic potassium channel opener targeting the final voltage sensor transition. 2162 47

The case of a 26-year-old woman with congenital long QT syndrome and recurrent arrhythmic syncope which had been misdiagnosed as a seizure disorder is presented. Useful criteria for discriminating between loss of consciousness due to congenital long QT syndrome and loss of consciousness caused by seizure activity are discussed. The multiple potential causes and clinical implications of a prolonged QT interval, as well as the clinical features and management of congenital long QT syndrome are reviewed.
J Gen Intern Med 2011 Dec
PMID:A 26-year-old woman with recurrent loss of consciousness. 2173 97

Hypoglycemia is a biochemical abnormality and often the rate-limiting step in the treatment of both type 1 and type 2 diabetes mellitus. Left uncorrected and prolonged, hypoglycemia can result in neuronal dysfunction and death, with deficits ranging from measurable cognitive impairments to aberrant behavior, seizures and coma. In this case report, hypoglycemia resulted in severe and persistent neurological (slurred speech and gait abnormalities), cognitive (inattention, disorientation and memory deficits) and behavioral manifestations (verbal hostility and irritability). It highlights the potentially severe neuropsychiatric sequelae following hypoglycemia and is timely for clinicians to be reminded that hypoglycemia prevention needs to be more of a focus of diabetes care in general.
Gen Hosp Psychiatry
PMID:Persistent, severe hypoglycemia-induced organic brain syndrome with neurological sequelae: a case report. 2176 45

Stroke is the leading cause of disability and one of the most common causes of death worldwide. Outside the setting of acute management, secondary prevention and stroke rehabilitation, little has been written to address the ongoing symptomatic and palliative needs of these patients and their families. In this literature review, we look beyond secondary prevention with the aim of providing evidence-informed management guidelines for the myriad and often under-recognized symptomatic and palliative care needs of stroke survivors. Some of the most common and disabling post-stroke symptoms that are reviewed here include central post-stroke pain, hemiplegic shoulder pain, painful spasticity, fatigue, incontinence, post-stroke seizures, sexual dysfunction, sleep-disordered breathing, depression and emotionalism. We review the role of caregivers and explore ways to support them and, lastly, remind the reader to be perceptive to the patient's spiritual needs. The literature is most robust, including controlled trials, for central post-stroke pain and depression. Synthesis and discussion outside these areas are frequently limited to smaller studies, case reports and expert opinion. While some data exists to guide informed decision-making, there is an urgent need to document best practice and identify appropriate clinical standards for the full spectrum of symptoms experienced by stroke survivors. We present the current and established data to aid health care providers in symptomatic and palliative management of stroke survivors.
J Gen Intern Med 2012 Jul
PMID:Symptomatic and palliative care for stroke survivors. 2252 22

Venlafaxine is a relatively new antidepressant with selective effects. Compared with traditional antidepressants, this agent has fewer adverse side effects. However, venlafaxine overdose has been reported with severe complications such as seizure, ventricular tachycardia, serotonin syndrome, neuroleptic malignant syndrome and rhabdomyolysis. We present a 21-year-old female with bipolar depression who took a low dose of venlafaxine, but subsequently developed severe rhabdomyolysis. Her plasma level of creatine kinase increased up to 18,711 U/L in few days. These findings may serve as a reminder to physicians to be alert to the possibility of rhabdomyolysis in patients who have only taken a low dose of venlafaxine.
Gen Hosp Psychiatry
PMID:Low-dose venlafaxine-induced severe rhabdomyolysis: a case report. 2245 96

There is limited literature reporting clozapine-associated stuttering. In this case report, we present a case of a young male who developed stuttering with clozapine, which improved with dose reduction. Computer-assisted searches on clozapine-induced stuttering yielded 16 cases, and analysis of these case reports suggests that stuttering may be linked to seizures or movement disorders, but other putative mechanisms may be at work, which need further research.
Gen Hosp Psychiatry
PMID:Clozapine-induced stuttering: a case report and analysis of similar case reports in the literature. 2251 17


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